Tubulointerstitial fibrosis is the final common pathway in late-stage renal disease. The pathogenesis of kidney fibrosis is characterized by overproduction and deposition of extracellular matrix (ECM), which ultimately leads to fibrotic lesions and tissue scarring. Renal interstitial fibroblasts are the principal effector cells that are responsible for ECM overproduction in the fibrotic kidney, and their activation is regarded as a key event in the pathogenesis of chronic renal fibrosis. Although the mechanism of myofibroblast activation and the fibrogenesis under various pathological conditions have not been completely understood, activation of multiple cytokines/growth factor receptors is involved in these processes.